Elevated levels of histamine cause the secretion of gastric hydrochloric acid (HCl), leading to gastrointestinal (GI) disorders and anxiety. While aberrant levels of histamine mediate neuroinflammation, pathogenic alterations in the hippocampus of the brain have been linked to anxiety. Eventually, antihistamine drugs that are used against GI disorders appear to be anxiolytic agents. Ranitidine is a widely used antihistamine drug to manage GI disorders as it works by blocking the histamine (H)-2 receptors in oxyntic cells thereby, reducing the HCl production in the stomach. Though some reports indicate the neuroprotective effects of ranitidine, its role against GI disorders related to anxiety remains unclear. Therefore, we investigated the effect of ranitidine against anxiety-related behaviors, neuronal density, and signs of microglia activation in the hippocampal CA3 region of cysteamine HCl-induced mouse model of GI disorder. Results obtained from the open field test (OFT), light and dark box test (LDBT), and elevated plus maze (EPM) revealed that ranitidine treatment reduces anxiety-like behaviors in experimental animals. Nissl staining and immunohistochemical assessment of Iba-1 positive microglia in the cryosectioned brains revealed that the ranitidine treatment enhances the density of pyramidal neurons in association with reduced activation of microglia in the CA3 region of the hippocampus of experimental mice.

In this paper, a system of searching for optimal paths is developed and concreted on a FPGA. It is based on a memristive emulator, used as a delay element, by configuring the test graph as a memristor network. A parallel algorithm is applied to reduce computing time and increase efficiency. The operation of the algorithm in Matlab is checked beforehand and then exported to two different Intel FPGAs: a DE0-Nano board and an Arria 10 GX 220 FPGA. In both cases reliable results are obtained quickly and conveniently, even for the case of a 300x300 nodes maze.

Women are at higher risk of cognitive impairment and Alzheimer’s disease (AD) after menopause when the estrous cycle becomes irregular and begins to taper off. Numerous studies have shown that estrogen deficiency, especially estradiol (E2), has been shown to play a key role in this phenomenon. Recently, a novel polymeric drug, hyaluronic acid-17β-Estradiol conjugate (HA-E2), has been developed which has the ability to cross the blood-brain barrier (BBB), facilitate a longer E2 release profile and lower risk of estrogen supplement related side effects. In this study, we used an ovariohysterectomy (OHE) rat model of postmenopausal cognitive deficits and explore whether HA-E2 treatment can improve the cholinergic septo-hippocampal innervation system, synaptic transmission in the hippocampal pyramidal neuron and cognitive impairment. Our results show that OHE rats after HA-E2 administration have increased expression of choline acetyltransferase (ChAT) in the medial septal nucleus (MS nucleus) and the hippocampus, increased spine density in hippocampal pyramidal neurons, and improved spatial learning and memory. Therefore, HA-E2 has great potential as a new novel class of drugs for estrogen-deficiency-induced cognitive impairment and AD.

Alzheimer’s disease (AD) causes dementia and memory loss in the elderly. Deposits of beta-amyloid peptide and hyperphosphorylated tau protein are present in AD’s brain. A filtrate of Helicobacter pylori’s culture was previously found to induce hyperphosphorylation of tau in vivo, suggesting that bacterial exotoxins could permeate the blood brain barrier and directly induce tau’s phosphorylation. H. pylori, which infects ~60% of the world population and causes gastritis and gastric cancer, produces a pro-inflammatory urease (HPU). Here the neurotoxic potential of HPU was investigated in cultured cells and in rats. SH-SY5Y neuroblastoma cells exposed HPU (50-300 nM) produced reactive oxygen species (ROS) and had an increased [Ca2+]i. HPU-treated BV-2 microglial cells produced ROS, cytokines IL-1β and TNF-α, expressed Iba1 and showed reduced viability, consistent with a neurotoxic effect of HPU. Rats received daily i.p. HPU (5 µg) for 7 days. Hyperphosphorylation of tau at Thr205, Ser199 and Ser396 sites was seen in hippocampal homogenates of treated rats, with no alterations in total tau or GSK-3b levels. HPU was not detected in the brain homogenates. Behavioral tests were performed to assess cognitive impairments. Our findings support previous data suggesting an association between infection by H. pylori and tauopathies such as AD, possibly mediated by its urease.